Multiple organ dysfunction after remote circulatory arrest: Common pathway of radical oxygen species?

Avi A. Weinbroum*, Edith Hochhauser, Valery Rudick, Yoram Kluger, Ela Karchevsky, Eran Graf, Bernardo A. Vidne

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Objectives: Cardiovascular, respiratory, and vascular dysfunction can follow trauma-induced no-flow-reflow states: hemorrhage, blunt trauma, or neurogenic shock. Liver ischemia- reperfusion (IR) induces remote lung damage by means of xanthine oxidase (XO) pro-oxidant activity. This damage was not proven in the heart, neither was the independent role of radical oxygen species (ROS) established in such cases. We investigated whether multiple organ dysfunction after a trauma-like IR is XO and ROS related and whether clinically used ROS scavengers could be beneficial. Methods: A controlled, randomized trial in which isolated rat livers, hearts, lungs, and aortic rings were perfused with Krebs-Henseleit solutions. After stabilization, livers were either perfused or made ischemic (2 hours). Then, pairs of liver plus heart, lung, or ring were reperfused in series (15 minutes), and then the second organ circulated alone for 45 minutes. Remote organ protection against the pro-oxidant hepatic-induced toxicity was evaluated by using allopurinol (1 mmol/L, heart), mannitol (0.25 g/kg, lung), or methylene blue (40 mg/kg, ring). Results: IR liver effluents typically contained high lactate dehydrogenase, XO, and uric acid concentrations compared with control organs. IR was associated with doubled lung peak inspiratory pressure and reduced static compliance. Myocardial velocity of contraction and relaxation decreased by one third of baseline, and rings contracted abnormally and responded inadequately to phenylephrine. Wet-weight to dry-weight ratios in the remote organs increased as well. Most remote reperfusion injuries were attenuated by the drugs. Conclusion: Liver no-flow-reflow directly induces myocardial, pulmonary, and vascular dysfunction. These are likely mediated by XO and ROS. The tested drugs protected against these pro-oxidants, even in the presence of circulating XO.

Original languageEnglish
Pages (from-to)691-698
Number of pages8
JournalJournal of Trauma and Acute Care Surgery
Issue number4
StatePublished - Oct 1999
Externally publishedYes


  • Inspiratory pressure
  • Ischemia-reperfusion
  • Myocardial contractility
  • Posttrauma
  • Radical oxygen species
  • Static compliance
  • Vascular tone, Aortic contraction
  • Xanthine oxidase


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